Novel therapeutic approach for heart failure by suppression of mitochondrial translocation of GSK-3beta

通过抑制 GSK-3beta 线粒体易位治疗心力衰竭的新方法

• 批准号: 26461132
• 负责人: Tanno Masaya
• 金额: $ 3.08万
• 依托单位: Sapporo Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2014
• 资助国家: 日本
• 起止时间: 2014-04-01 至 2017-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26461132/
• 关键词: ミトコンドリア透過性遷移孔; 細胞死; グリコーゲン合成酵素キナーゼ3beta; グリコーゲン合成酵素キナーゼ3β; GSK-3β

项目成果

ROS-induced mitochondrial translocation of phosphatases cancelscell-protective signals activated by phosphorylation of mitochondrial protective kinases

ROS诱导的线粒体磷酸酶易位消除了线粒体保护激酶磷酸化激活的细胞保护信号

• 发表时间: 2016
• 作者: Ohwada W;Tanno M;Yano T;Kuno A;Miki T;Ishikawa S;Tatekoshi Y;Abe K;Ohno K;Mizuno M;Nakata K;Miura T.
• 通讯作者: Miura T.

Excessive degradation of adenine nucleotides by up-regulated AMP deaminase underlies afterload-induced diastolic dysfunction in the type 2 diabetic heart

• DOI: 10.1016/j.yjmcc.2015.01.004
• 发表时间: 2015-03-01
• 期刊: JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
• 影响因子: 5
• 作者: Kouzu, Hidemichi;Miki, Takayuki;Miura, Tetsuji
• 通讯作者: Miura, Tetsuji

Mitochondrial translocation of GSK-3β, a trigger of mitochondrial permeability transition, is mediated by its N-terminal domain and promoted by interaction with VDAC2.

GSK-3β 的线粒体易位是线粒体通透性转变的触发因素，由其 N 末端结构域介导，并通过与 VDAC2 的相互作用促进。

• 发表时间: 2014
• 作者: Tanno M;Ishikawa S;Miki T;Kuno A;Kouzu H;Yano T;Miura T
• 通讯作者: Miura T

Depletion of fructose 1,6-diphosphate but not post-translational modification plays a major role in activation of AMP deaminase in diabetic hearts: a novel mechanism for diabetic cardiomyopathy.

果糖 1,6-二磷酸的消耗而不是翻译后修饰在糖尿病心脏中 AMP 脱氨酶的激活中发挥着重要作用：糖尿病心肌病的一种新机制。

• 发表时间: 2016
• 作者: Y. Tatekoshi;M. Tanno;A. Kuno;S. Ishikawa;T. Yano;T. Miki;M. Ogasawara;T. Tobisawa;K. Ohno;S. Muratsubaki;K. Nishizawa;T. Miura
• 通讯作者: T. Miura

Continuous erythropoietin receptor activation reverses increased myocardial susceptibility to ischemia/reperfusion injury in chronic renal failure.

持续的促红细胞生成素受体激活可逆转慢性肾功能衰竭中心肌对缺血/再灌注损伤的敏感性增加。

• 发表时间: 2015
• 作者: K. Nishizawa;T. Yano;T. Miki;M. Tanno;A. Kuno;H. Kouzu;T. Tobisawa;M. Mizuno;H. Sugawara;T. Miura.
• 通讯作者: T. Miura.